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VPS33B negatively modulated by nicotine functions as a tumor suppressor in colorectal cancer

Yiyu Chen1,2, Zhen Liu3, Huijun Wang2

  • 1Cancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong, China.

International Journal of Cancer
|May 25, 2019
PubMed

Insights

Vacuolar protein sorting 33B (VPS33B) acts as a tumor suppressor in colorectal cancer (CRC), with its downregulation linked to poor prognosis. VPS33B interacts with NESG1 to inhibit CRC progression and metastasis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • The role of vacuolar protein sorting 33B (VPS33B) in colorectal cancer (CRC) remains largely uncharacterized.
  • VPS33B is implicated in various cellular processes, but its specific function in CRC pathogenesis is unknown.

Purpose of the Study:

  • To investigate the biological role of VPS33B in colorectal cancer.
  • To elucidate the molecular mechanisms underlying VPS33B's function and its potential as a therapeutic target.

Main Methods:

  • Utilized dextran sulfate sodium/azoxymethane (DSS/AOM)-induced CRC mouse models and nicotine-treated CRC cells.
  • Employed in vivo and in vitro experiments to assess the effects of VPS33B overexpression on CRC proliferation, metastasis, and chemoresistance.
  • Investigated the interaction between VPS33B and NESG1 using colocalization studies and analyzed their impact on signaling pathways.

Main Results:

  • VPS33B was found to be downregulated in CRC models and cells, correlating with poor patient prognosis.
  • VPS33B overexpression suppressed CRC proliferation, intrahepatic metastasis, and cisplatin resistance by modulating the EGFR/RAS/ERK/c-Myc/p53/miR-133a-3p feedback loop.
  • VPS33B interacted with the tumor suppressor NESG1, collectively inhibiting CRC malignant phenotypes via the RAS/ERK/c-Jun pathway.

Conclusions:

  • VPS33B functions as a tumor suppressor in colorectal cancer, easily dysregulated by chemical carcinogens.
  • VPS33B and NESG1 interact to suppress CRC progression by modulating key signaling pathways and feedback loops.
  • VPS33B represents a potential therapeutic target for colorectal cancer treatment.
Keywords:
EGFR/RAS/ERK/c-Myc/p53/miR-133a-3p feedback loopNESG1VPS33Bchemical carcinogenscolorectal cancer

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